
Interleukin 1β Blockade Reduces Intestinal Inflammation in a Murine Model of Tumor Necrosis Factor–Independent Ulcerative Colitis
Author(s) -
Marina Liso,
Giulio Verna,
Elisabetta Cavalcanti,
Stefania De Santis,
Ricardo L. Armentano,
Angela Tafaro,
Antonio Lippolis,
Pietro Campiglia,
Antonio Gasbarrini,
Mauro Mastronardi,
Theresa T. Pizarro,
Fabio Cominelli,
Loris Riccardo Lopetuso,
Marcello Chieppa
Publication year - 2022
Publication title -
cmgh
Language(s) - English
Resource type - Journals
ISSN - 2352-345X
DOI - 10.1016/j.jcmgh.2022.03.003
Subject(s) - medicine , anakinra , tumor necrosis factor alpha , ulcerative colitis , inflammatory bowel disease , colitis , cytokine , immunology , inflammation , interleukin , infliximab , gastroenterology , disease
Inflammatory bowel diseases are multifactorial diseases commonly treated with either immunomodulatory drugs or anti-tumor necrosis factor (TNF). Currently, failure to respond to anti-TNF therapy (assessed no earlier than 8-12 weeks after starting treatment) occurs in 20%-40% of patients enrolled in clinical trials and in 10%-20% in clinical practice. Murine models of inflammatory bowel disease provide important tools to better understand disease mechanism(s). In this context and among the numerous models available, Winnie-TNF-knockout (KO) mice recently were reported to show characteristics of ulcerative colitis (UC) that are independent of TNF, and with increased interleukin (IL)1β production.